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Results for “Lipid Mobilization”

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At least 199 records · Page 11Linked to original sources
PubMed1984

The effects of synthetic locust adipokinetic hormone on dispersed locust fat body cell preparations: cAMP induction, lipid mobilization, and inhibition of protein synthesis.

A procedure for the preparation of functional cells from adult locust fat bodies by collagenase treatment has been developed. The high variability of replicates encountered when whole fat bodies are incubated in vitro is greatly reduced in incubation of the dispersed cells. Synthetic locust adipokinetic hormone (AKH) (40 nM) stimulated release of lipids from the dispersed fat body cells at a rate comparable to that observed using whole fat bodies in vitro. Synthetic AKH elevated cAMP levels sixfold in dispersed cells. In addition, AKH inhibited protein synthesis to a maximum of 50-70% in a concentration-dependent manner. None of these actions of AKH required the presence of locust hemolymph components. These results demonstrate the utility of the isolated locust fat body cells for investigating hormonal action in vitro.

Adipose Tissue↗
PubMed1980

A lipid mobilizing factor in serum of tumor-bearing mice.

There is considerable evidence that the growing tumor requires a source of unsaturated fatty acids, but the nature of this source and the mechanism of mobilizing the fatty acids from it are obscure. These experiments make use of AKR mice with implanted adipose tissue labeled with 1-14C linoleic acid. With this experimental animal, it has been found that: (a) in the normal, fed mouse, fat is mobilized slowly and appears largely as respiratory CO2, following oxidation, (b) in the normal, fasted mouse, fat is mobilized rapidly and appears largely as respiratory CO2; (c) in the tumor-bearing, fed mouse, fat is mobilized rapidly and appears largely in the tumor; and (d) the serum from tumor-bearing mice, when injected into normal mice, produces an immediate massive fat mobilization that does not respond to feeding, whereas the serum from normal, fed mice does not. It is concluded that a mobilizing factor of unknown nature is present in the serum of tumor-bearing AKR mice.

Adipose Tissue↗
PubMed1993

Mismatch between lipid mobilization and oxidation: glycerol kinetics in running African goats.

Glycerol kinetics and total fatty acid (FA) oxidation of trained African pygmy goats were measured by continuous infusion of [2-3H]glycerol and indirect calorimetry during treadmill exercise at 40, 60, and 85% maximal O2 consumption (VO2max). Our main goals were 1) to determine whether rates of FA mobilization and utilization are eventually matched as exercise intensity increases, thereby minimizing reesterification to supply more FA to working muscles, and 2) to test the hypothesis that lipolytic rate is proportional to aerobic capacity by comparing low-aerobic goats with published values from highly aerobic dogs and humans. Mean rate of glycerol release in the circulation (Ra glycerol) was 3.83 +/- 0.11 at rest, 7.69 +/- 0.88 at 40% VO2max, reached a maximum of 15.32 +/- 0.95 at 60% VO2max, and returned to 10.53 +/- 0.76 mumol.kg-1 x min-1 at 85% VO2max. Lipolytic rate did not match total FA oxidation, implying that Ra glycerol cannot be used as an index of FA utilization, even during intense exercise. A large fraction of total FA released by lipolysis was reesterified at 60 and 85% VO2max, showing that FA mobilization does not limit whole animal FA oxidation at these intensities. Comparing goat, dog, and human responses reveals that mammalian lipolytic rate is scaled with aerobic capacity. High- and low-aerobic species exercising at the same %VO2max mobilize FA in exact proportion with their metabolic rate, suggesting that the relative contribution of FA to total energy provision is independent of VO2max.

Animals↗
PubMed1975

Role of growth hormone in lipid mobilization stimulated by prolonged muscular exercise in the rat.

The effects of prolonged muscular exercise (swim in tepid water for 60 min) on blood glucose, plasma FFA and R-GH were studied in a group of normal rats and the effect on blood glucose and plasma FFA in a group of hypophysectomized rats. The data obtained showed that, whereas in normal rats plasma FFA rose after muscular exercise, plasma R-GH fell sharply. In Hypophysectomized rats, however, muscular exercise did not increase plasma FFA levels.

Animals↗
PubMed1975

[Studies on lipid mobilization in obesity without glucose intolerance. 1st communication. Noradrenaline-stimulated lipolysis].

1. In obese patients with normal glucose tolerance the norepinephrine-induced lipolysis in vivo was significantly higher as compared with a non-obese group. This was observed both during weight-related and constant norepinephrine infusion. 2. In the obese group a discordant release of free fatty acids and glycerol and a significantly lower quotient of FFA/Glycerol than in the controls was found. It is supposed that in obesity the re-esterification of FFA is increased.

Adipose Tissue↗
PubMed1988

Mechanism of the lipid-mobilizing effect of alpha-2 adrenergic antagonists in the dog.

Alpha-2 adrenergic antagonists may constitute putative antiobesity agents. These drugs may act: 1) by blockade of the antilipolytic alpha-2 adrenoceptor on fat cell membranes and 2) by activation of the sympathetic adrenergic system (blockade of central and presynaptic alpha-2 adrenoceptors). Studies were undertaken in the dog, a species possessing fat cell alpha-2 and beta-adrenoceptors in order: 1) to define and compare the metabolic and endocrinological impacts of recently discovered alpha-2 antagonists [idazoxan and SK&F 86,466 (6-chloro-N-methyl-2,3,4,5-tetrahydro-1H-3-benzazepine)] and of an older one (yohimbine) and 2) to dissociate the contribution of the noradrenergic activation from a postsynaptic action on fat cell and endocrine pancreas alpha-2 adrenoceptors. Binding studies showed that the three compounds have similar affinities for the alpha-2 adrenoceptor on both cerebrocortical and fat cell membranes. Their ability to suppress the antilipolytic effect of an alpha-2 agonist [UK-14,304 (5-bromo-6-(2-imidazolin-2-ylamino)-quinoxaline)] on isolated fat cells was equivalent. Yohimbine perfusion induced a dose-dependent increase in plasma nonesterified fatty acids (NEFA) and immunoreactive insulin concentrations. At equivalent doses, the three alpha-2 adrenergic antagonists induced NEFA mobilization, increase in immunoreactive insulin and norepinephrine plasma levels with an order of potency: yohimbine much greater than idazoxan greater than or equal to SK&F 86,466. The weakest effect on sympathetic activation was with SK&F 86,466. The effects of yohimbine were suppressed completely by pretreatment with propranolol. Clonidine infusion reduced NEFA levels in dogs. Yohimbine but not SK&F 86,466 abolished completely this lowering effect of clonidine on NEFA and glycerol levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1976

[Lipid mobilization in obesity without carbohydrate intolerance. 2. Caffeine-stimulated lipolysis].

The lipolysis induced by i.v. injection of caffeine (3 mg/kg body weight) has been investigated in 11 normal subjects and 18 obese patients with normal 50 g oral glucose tolerance test and normal thyroid-function. The pattern of blood-glucose and immunoreactive insulin (IRI) secretion were not influenced by caffeine in both groups. Both in the controls and obese group a significant response of FFA and glycerole were noted. In the obese group the caffeine-induced lipolysis was slightly higher as compared with controls. There are no differences in FFA-response between obese group and controls. The observations suggest that an impaired lipolysis is not a pathogenetic factor for development of obesity.

Adult↗
PubMed1995

Analysis of the interactions between growth hormone and metaproterenol on lipid mobilization.

The possible modification of the in vitro lipolytic action of rat growth hormone (rGH) or a mixed beta-adrenergic agonist (metaproterenol) on rat adipose tissue after a previous acute treatment with these compounds was assessed by measuring glycerol release from adipocytes. The involvement of adenosine deaminase (ADA) and dexamethasone, was also considered. The results showed that the previous acute treatment with rGH or the beta-adrenergic agonist did not alter the in vitro rGH or metaproterenol lipolytic response. The presence of ADA at a non-lipolytic concentration per se (0.02 U/ml) potentiated the lipolytic response of both compounds. Also, the addition of non-lipolytic concentrations of dexamethasone (0.5 microM) or beta-adrenergic agonist (10(-7)M) to the incubation medium potentiated the rGH lipolytic response, while the metaproterenol-induced glycerol release was not affected by the simultaneous addition of a rGH concentration (2 x 10(-7) M) which had no lipolytic effect per se.

Adenosine Deaminase↗
PubMed1981

Exercise and the cAMP system in rat adipose tissue. I. Lipid mobilization.

Protein kinase (PK) and hormone-sensitive lipase (HSL) were measured at rest in adipose tissue of untrained male rats and in that of animals subjected to a strenuous program of treadmill running. Total amounts of PK activity (decreased from 860 +/- 104 to 474 +/- 53 pmol.min-1. (10(6) cells)-1 (P less than 0.01) as a result of exercise training. At the same time, binding capacity for adenosine 3',5'-cyclic monophosphate (cAMP) was elevated in the runners. These data suggest a functional loss in catalytic activity without a loss in binding capacity. In addition, the results provide evidence that the capacity of PK to activate HSL is reduced in adipocytes of physically trained rats. HSL activity was measured in both adipose tissue slices and isolated adipocytes. The results show that the levels of activity of HSL did not increase as a result of the running program. These results provide evidence that the lipolytic capacity of adipocytes of normal untrained male rats is sufficiently large to meet the increased demand for free fatty acids imposed by the exercise program without the need for an adaptive increase in HSL activity.

Adipose Tissue↗
PubMed2005

Effect of eicosapentaenoic acid (EPA) on expression of a lipid mobilizing factor in adipose tissue in cancer cachexia.

Adipose tissue of mice bearing a cachexia-inducing murine tumour (MAC16) shows increased expression of zinc-alpha(2)-glycoprotein (ZAG), a lipolytic factor thought to be responsible for the increased lipolysis. The anti-cachectic agent eicosapentaenoic acid (EPA) (0.5 g/kg) attenuated the loss of body weight in mice bearing the MAC16 tumour, and this was accompanied by downregulation of ZAG expression in both white and brown adipose tissue, as determined by Western blotting. Glucocorticoids may be responsible for the increased ZAG expression in adipose tissue. Dexamethasone (1.68 microM) stimulated lipolysis in 3T3-L1 adipocytes, and this effect was attenuated by EPA (50 microM). In addition the lipolytic action of dexamethasone was attenuated by anti-ZAG antibody, suggesting that the induction of lipolysis was mediated through an increase in ZAG expression. This was confirmed by Western blotting, which showed that dexamethasone (1.68 microM) induced a two-fold increase in ZAG expression in both cells and media, and that this was attenuated by EPA (50 microM). These results suggest that EPA may preserve adipose tissue in cachectic mice by downregulation of ZAG expression through interference with glucocorticoid signalling.

3T3-L1 Cells↗